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Sys Path II > Intestine > Flashcards

Intestine Flashcards

1
Q

What is the lifecycle of an enterocyte?

A
  • mature enterocytes are tall & columnar w/ luminal microvilli which contain a surface glycocalyx that houses the digestive & absorptive enzymes
  • the mature cells do not proliferate
  • enterocytes move up the crypt & intestinal villus to the extrusion zone at the villus tip, where effete enterocytes are discarded into the fecal mass by apoptosis
  • turnover rate for enterocytes is rapid
  • in 3-week-old pigs turnover rate is 2-3 days
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2
Q

What are the epithelial cells of the intestine?

A
  • enterocytes
  • undifferentiated or crypt epithelial cells
  • goblet cells
  • paneth cells
  • enteroendocrine cells
  • M cells
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3
Q

what do undifferentiated or crypt epithelial cells do?

A
  • they have no digestive capacity
  • they are the progenitor cells that replace all other epithelial cell types
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4
Q

What do goblet cells do?

A
  • secrete mucus
  • their numbers tend to increase aborally throughout the length of the intestine
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5
Q

What do paneth cells do?

A
  • located near the crypt base (present in primates, horses, rodents, & possibly swine)
  • unlike all the other cells of the intestinal surface, these cells migrate toward the crypts rather than the villus tips
  • they produce bactericidal substances (cryptdin & lysins) which protect proliferating crypt cells from infection
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6
Q

What do enteroendocrine cells do?

A
  • in the crypts produce & secrete into surrounding tissue (not into intestinal lumen) serotonin, gastrin, cholecystokinin, etc. which coordinate function (secretion, peristalsis, & digestion) of GIT
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7
Q

What do M cells do?

A

cover the gut associated lymphoid tissue (GALT) & serve important functions in the uptake of antigens from the intestinal lumen

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8
Q

What does lymphoid tissue do in the intestines?

A
  • the intestinal lymphoid tissue represents 25% of the total body’s lymphoid mass in most animals
  • normal gut does not response to normal food antigens, in spite of the fact that the average person ingests ~70,000 kg of antigens in a lifetime
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9
Q

How does postmortem autolysis of the intestinal mucosa affect necropsy of the intestines?

A
  • rapidly results in loss of superficial intestinal villar epithelium which interferes w/ histological detection of certain important pathogens (ex: cryptosporidia, E. coli) & diagnosis of villar atrophy (both v important for diagnostics of neonatal D+)
  • hence, for diagnostics of neonatal D+, it is highly recommended to perform necropsy on an animal that just died (or was just euth’d)
  • swine practitioners often submit live piglets w/ D+ to diagnostic lab (if at all possible), which will be euth’d immediately before necropsy to avoid autolytic changes in intestines
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10
Q

How to necropsy intestines?

A
  • strive to obtain formalin fixed intestinal samples as soon as possible & then proceed w/ the standard necropsy exam
  • standard exam: varies according to sp
  • important to systemically examine in situ the external surface & position of the entire GIT (dx adhesions, torsions, displacements, etc.) & then examine mucosa & contents of each portion of GIT w/ associated LNs & mesentery
  • sample collection for microbiology (refrigerated or frozen) & pathology (formalin fixed) should be collected from each portion of GIT
  • common error is placing too much tissue in too little formalin - “rule of thumb” is 10:1 formalin to tissue ratio
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11
Q

What are developmental anomalies of the intestines?

A
  • atresia
  • megacolon
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12
Q

What is atresia?

A

congenital absence of a normal opening or normal patent lumen (ex: atresia ani, atresia coli, etc.)

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13
Q

What is megacolon?

A
  • a large distended colon filled w/ feces
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14
Q

what is congenital megacolon?

A
  • inappropriate innervation (lack of myenteric plexuses) in pigs, dogs, cats, overo foals, & humans
  • atresia ani can also result in megacolon
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15
Q

What is acquired megacolon?

A
  • secondary to damage to the colonic innervation; occasionally happens in Car hit by a car
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16
Q

What is ileus?

A
  • hypomotility resulting in a functional obstruction of the bowel
  • there are no gross lesions other than atonic dilation of the intestine
  • it occurs in all spp
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17
Q

What are the causes of ileus?

A
  • post-surgical due to bowel manipulation at surgery
  • peritonitis from any cause
  • severe abdominal pain
  • electrolyte imbalances (esp. hypokalemia)
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18
Q

What are some causes of mechanical intestinal obstruction?

A
  • enteroliths occasionally in Eq
    -trycho- & phytobezoars in rumen
  • feed impaction
  • cecal impaction
  • sand colic
  • linear foreign bodies
  • intestinal stricture
  • intussusception
  • rectal prolapse secondary to tenesmus or excessive postpartum straining
  • intestinal volvulus, torsion, & strangulation
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19
Q

Which spp does feed impaction occur in?

A

All of them

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20
Q

Who does cecal impaction occur in and why?

A
  • old horses b/c of high roughage diet or poor dentition
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21
Q

Who does sand colic occur in and why?

A
  • large amounts of ingested sand can accumulate anywhere in the equine colon, resulting in impaction
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22
Q

Who do linear foreign bodies occur most commonly in?

A

carnivores

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23
Q

What are intestinal strictures the result of?

A

healing w/ scarring & fibrosis:
- post-enterotomy healing -> fibrosis -> stricture
- rectal stricture

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24
Q

Pathogenesis of rectal strictures?

A
  • recurrent rectal prolapse can result in circumferential necrosis & subsequent fibrosis -> stricture
  • salmonellosis in pigs -> thrombosis of the cranial hemorrhoidal artery (lack of collateral circulation) -> necrosis -> circumferential fibrosis -> stricture
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25
Q

What is intussusception?

A
  • when one segment of intestine becomes telescoped into the immediately distal segment of intestine
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26
Q

What are the clinical features of intussusception?

A
  • similar to those of intestinal obstruction & venous infarction (in more severe cases)
  • red to black discolouration depends on the degree of vascular compromise, ranging from congestion & edema to hemorrhage & necrosis
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27
Q

What is the intussusceptum?

A

the trapped segment

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28
Q

What is the intussuscipiens?

A

the enveloping portion of the intestine

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29
Q

What is the cause of intussusception?

A

generally unknown but is thought to be associated w/ intestinal irritability & hypermotility due to enteritis or intestinal parasites

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30
Q

What can spontaneously happen w/ intussusceptions?

A
  • can spontaneously reduce by sloughing of the infarcted mucosa, which is passed in the feces
  • the site of sloughing is repaired by granulation tissue (due to loss of scaffold) resulting in a circumferential fibrosis/scar & intestinal stricture
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31
Q

How can you tell antemortem from postmortem intussusceptions?

A
  • b/c peristalsis continues after death, intestinal invaginations can occur postmortem
  • POSTMORTEM (OR TERMINAL) INVAGINATIONS ARE EASILY REDUCED, THERE IS NO VASCULAR COMPROMISE (EDEMA, CONGESTION, HEMORRHAGE), NO ADHESIONS (PERITONEAL SURFACES ARE SMOOTH & GLISTENING), & NO NECROSIS
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32
Q

What is rectal prolapse a type of?

A

intussusception

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33
Q

What is volvulus ?

A

twisting of the intestine on its mesenteric axis

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34
Q

What is torsion?

A

rotation of the abomasum, colon, or cecum along its long axis

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35
Q

What is intestinal strangulation ?

A
  • occurs in Eq w/ pedunculated lipomas which wrap around the intestinal mesentery or the bowel, causing ischemia, colic, & death
  • pedunculated lipomas may rotate about their pedicle cutting off their own blood supply
  • when this occur, they undergo necrosis & mineralization
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36
Q

What are internal hernias?

A
  • displacements of intestine through a normal or pathologic foramen in the abdominal cavity
  • most common of these occur in horses & include herniation through mesenteric tears & the epiploic foramen
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37
Q

what are external hernias?

A
  • formed when a hernial sac, formed by a pouch of parietal peritoneum, penetrates outside the abdominal cavity
  • types of external herniation include umbilical, diaphragmatic, hiatal, inguinal, scrotal, & perineal
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38
Q

In which types of hernias does intestinal incarceration occur?

A

both internal & external

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39
Q

What happens when volvulus, torsion, strangulation, intussusception, or incarceration results in the compression of a the mesenteric vesseles?

A

-> resulting in ischemic necrosis (infarction)
- venous infarction is a result of occlusion of the thin-walled mesenteric veins
- b/c the arterial supply is anatomically more resistant to occlusion, blood is pumped into the twisted segment but cannot drain
- TRANSMURAL CONGESTION, EDEMA, HEMORRHAGE, & EVENTUAL NECROSIS (VENOUS INFARCTION) WILL RESULT

40
Q

what happens at surgery or necropsy w/ intestinal venous infarction?

A
  • the twisted segment of intestine is distended w/ gas & hemorrhagic fluid & is discoloured dark red to black
  • there is a SHARP LINE OF DEMARCATION btwn the affected & normal intestine
  • during surgery, it is v important to determine the viability of the bowel after reduction of the volvulus
  • the affected/ dead segment of intestine remains dark red & thickened after reduction of the volvulus b/c of severe congestion & edema that progressed to hemorrhage & necrosis (venous infarction)
  • Intestinal stasis & toxemia &/or bacteremia & septicemia may result from bacterial overgrowth & anoxic bowel necrosis
  • toxemia & intestinal rupture may result in death
  • if reduction of a volvulus results in re-established circulation, reperfusion injury may also occur (mediated by oxygen free radicals, complement activation, & inflammation)
41
Q

What is iatrogenic rectal tearing?

A
  • may occur secondary to rectal palpation
  • presence of blood on a rectal sleeve after palpation is cause for concern b/c peritonitis may be the result of penetration to the peritoneal cavity
42
Q

What is “brown gut” (ceroidosis)?

A
  • rare condition caused by the accumulation of a brown ceroid pigment (formerly called lipofuscin) in the lysosomes of smooth muscle cells of the tunica muscularis
  • it does not cause any clinical signs but may be an indicator of a metabolic or nutritional disorder (vitamin E deficiency or high concentration of polyunsaturated fatty acids in the diet)
43
Q

What is muscular hypertrophy of the distal ileum?

A
  • an idiopathic segmental & circumferential thickening of the ileal tunica muscularis most commonly found in horses & pigs
  • in both species, it is often an asymptomatic lesion
44
Q

What is hemomelasma ilei?

A
  • another unique lesion in the horse
  • these are red, brown to black plaques on the ileal & jejunal subserosa
  • they are various stages of hemorrhage caused by larval migrations of strongyles (Strongylus edentatus)
  • they have no clinical significance
    however, they may provide a hint of an inadequate deworming program
45
Q

What is the pathogenesis of cranial mesenteric arteritis & thrombosis?

A
  • Strongylus vulgaris causes mesenteric arteritis & thrombosis in Eq
  • ingested larvae penetrate the large intestinal wall & migrate on or w/in the tunica intima (histo: tunica intima consists of endothelium, subendothelial CT, & an internal elastic mb) along the intestinal arterioles & arteries towards the cranial mesenteric root
  • larval migration causes vascular damage, inflammation, (verminous arteritis), thrombosis, intimal fibroplasia, & aneurysms
  • occasionally detached thromboemboli occlude downstream smaller intestinal arteries & cause local ischemia resulting in intermittent colic episodes, even though fatal incidents are rare most likely due to extensive collateral circulation
  • effective anthelmintics markedly reduced the prevalence of S. vulgaris infection in Eq
46
Q

What is lymphangiectasia?

A

(lacteal dilation)
- most common protein-losing enteropathy in Ca

47
Q

What are the clinical signs of lymphangiectasia?

A
  • D+, steatorrhea, hypoproteinemia -> ascites
48
Q

What are the causes of lymphangiectasia?

A
  • acquired secondary to lymph vessel obstruction caused by granulomatous or neoplastic diseases
  • sometimes, it is a part of chronic inflammatory bowel disease
  • congenital developmental disorder of the lymphatic vessels
49
Q

what is diarrhea?

A

abnormally frequent discharge of semisolid of fluid fecal matter

50
Q

What are the most important clinical consequences of D+?

A

DEHYDRATION & subsequent ACIDOSIS

51
Q

How can D+ lead to hypovolemic shock?

A

D+ -> dehydration -> hypovolemia -> hemoconcentration -> inadequate tissue perfusion & oxygen concentration -> inefficient energy generation in tissues by anaerobic glycolysis -> hypoglycemia leads to ketoacidosis -> acidosis is enhanced by fecal bicarbonate loss & by inadequate renal excretion of H+ ions & inadequate absorption of bicarbonate due to inadequate renal perfusion -> systemic increase in intracellular hydrogen ion concentration & a decrease in intracellular potassium ion concentration -> decrease in neuromuscular control of myocardial contraction -> further decrease in tissue perfusion -> vicious cycle culminates in hypovolemic shock

52
Q

How do you diagnose D+ on postmortem?

A
  • sunken eyes in orbits
  • subcutis is tacky
  • skin lacks elasticity (in fresh animals)
  • in piglets, urates precipitation may be present in the renal medulla
53
Q

What is D+ with normal intestines?

A
  • intestinal morphology is not affected but the animal has D+
54
Q

What are the different types of normal intestine D+?

A

secretory & osmotic

55
Q

What is the pathogenesis and etiology of secretory diarrhea?

A
  • enterotoxigenic E. coli (ETEC) infection in neonatal pigs, calves, lambs, & humans causes secretory D+
  • these bacteria are able to colonize the small intestinal enterocytes by way of their pilus antigens (fimbria), which anchor them to the enterocytes
  • thus these bacteria are not flushed out by peristalsis
  • the bacteria produce toxins that cause enterocytes to secrete water & electrolytes
  • the net result is D+
  • B/c the enterocytes are not damaged, NO LESIONS ARE OBSERVED, & absorption is functional
  • CHYLE IS PRESENT IN THE MESENTERIC LYMPHATIC VESSELS similar to animals w/o enteric disease, indicating that unlike the malabsorptive diseases of the small intestine, absorption proceeds normally in cases of enterotoxic colibacillosis
56
Q

What is the pathogenesis and etiology of osmotic diarrhea?

A
  • ruminal acidosis results in higher osmolarity of the gastrointestinal contents
57
Q

What is the pathogenesis of malabsorptive diarrhea?

A
  • caused by a decreased absorptive surface usually a consequence of damage to absorptive enterocytes, to microvilli on the surface of enterocytes, &/or to undifferentiated crypt cells
  • this is usually manifested as villous atrophy
  • the loss of the absorptive-digestive villous enterocytes causes maldigestion & malabsorption
  • furthermore, b/c ingesta & normal alimentary secretions are unabsorbed, they are degraded further & fermented in the intestine by bacteria, increasing the osmolarity of the intestinal contents, w/ a subsequent increase in the fluid content of the bowel
58
Q

What occurs w/ damage to mature absorptive enterocytes w/ malabsorptive D+?

A
  • destruction of these cells results in loss of enterocytes & villous atrophy
  • b/c the regenerative crypt cells are not attacked by pathogens w/ a tropism for villous enterocytes, disease w/ villous enterocyte damage are not necessarily fatal
  • the lost cells are replaced by the maturing cells migrating along the basement membrane from the crypt to the villous
  • the naked basement membrane stimulates contraction of the villi resulting in villous atrophy
  • the contraction may be a function of the smooth muscle in the lamina propria
  • the functionally immature migrating crypt cells cover the villi
  • often, these immature cells becomes squamoid (flat) in an effort to cover the maximum areas of basement mb
  • however, if ‘naked’ basement membranes of the adjacent villi contact each other, they will adhere, resulting not only in villous blunting but also in villous fusion, preventing the reformation/regeneration of normal villi
59
Q

What is the etiology of malabsorptive D+ with damage to mature absorptive enterocytes?

A

rotavirus, coronavirus, Cryptosporidium parvum

60
Q

What occurs w/ damage to undifferentiated crypt cells w/ malabsorptive D+?

A
  • loss of the undifferentiated epithelial cells in the base of the crypts means loss of the cells capable of rapid mitosis, & thus regeneration of the epithelium is impaired.
  • this type of loss is more severe & often fatal, compared w/ just the loss of villous enterocytes
60
Q

What is the etiology of malabsorptive D+ with damage to undifferentiated crypt cells?

A
  • parvovirus, BVD virus, rinderpest virus, & some mycotoxins
61
Q

What is the etiology of ulcerative enterocolitis?

A

Salmonella, Brachyspira, Lawsonia, bovine coccidiosis, Clostridium spp.

62
Q

What is the etiology of ulcerative enterocolitis?

A
  • microorganism cause extensive necrosis of superficial epithelium, lamina propria, &/or blood vessels
  • result is massive & acute necrohemorrhagic or fibrinonecrotic enteritis
  • absorptive surface is lost (malabsorption) & ulceration allows for loss of interstitial & plasma fluids
63
Q

What are other disorders (other than ulcerative colitis) of the intestinal mucosa that result in the loss of proteins due to increased intestinal permeability?

A

Johne’s disease, lymphangiectasia, lymphoma, etc.

64
Q

what are some non-intestinal causes of D+?

A
  • pancreatic insufficiency, pancreatitis, R-heart failure, ruminal acidosis, etc.
65
Q

What are common etiologies for infectious undifferentiated diarrhea in piglets younger than 3 wks?

A

rotavirus, coronavirus, ETEC, Isospora suis*

  • = may cause mortality
66
Q

What are common etiologies for infectious undifferentiated diarrhea in calves younger than 3 wks?

A

rotavirus, coronavirus, ETEC, & cryptosporidium

67
Q

What are etiologies for infectious undifferentiated diarrhea in lambs younger than 3 wks?

A

rotavirus (less common), coronavirus (rare), ETEC (less common), Cryptosporidium (rare)

68
Q

What are etiologies for infectious undifferentiated diarrhea in foals younger than 3 wks?

A

rotavirus (less common), coronavirus (rare), Cryptosporidium (rare)

69
Q

Which undifferentiated diarrhea causative agent in animals younger than 3 wks is zoonotic?

A

cryptosporidium

70
Q

What is undifferentiated neonatal D+?

A
  • this disease complex has SIMILAR clinical & gross pathological presentation despite being caused by different pathogens in neonates of various spp
71
Q

What are the clinical signs in all spp of undifferentiated neonatal D+?

A
  • variable degree of dehydration
  • weakness & potentially inappetence
  • if D+ is prolonged, weight loss
  • perineum stained w/ diarrheic feces
  • yellow pasty to watery diarrhea
  • usually high morbidity & variable mortality (depending on etiology)
  • no differentiating gross lesions
72
Q

What is seen on necropsy in all spp w/ undifferentiated neonatal D+?

A

nonspecific findings
- usually marked dehydration
- distended small intestines w/ watery contents which are present also in the entire colon
- stomach may or may not be filled w/ milk

73
Q

How do we diagnose all spp w/ undifferentiated neonatal D+?

A
  • final diagnosis usually needs additional lab tests to ID causative agents due to nonspecific (undifferentiated) clinical signs & gross pathology changes
  • MANY OF THE CAUSATIVE AGENTS OF UNDIFFERENTIATED NEONATAL D+ ARE ONLY TRANSIENTLY PRESENT IN THE SUPERFICIAL LAYERS OF THE INTESTINES (ex: SLOUGHED & EXCRETED w/ AFFECTED ENTEROCYTES) & are QUICKLY LOST DURING THE EARLY STAGES OF AUTOLYSIS
  • ACCORDINGLY, TO OVERCOME THESE OBSTACLES ONE OR MORE LIVE UNTREATED ANIMALS IN THE EARLY PHASE OF CLINICAL DISEASE & REPRESENTATIVE OF THE HERD PROBLEM, MUST BE EXAMINED & SACRIFICED TO ENSURE HIGH DIAGNOSTIC RATE
  • REGULAR NECROPSY PROCEDURE HAS TO BE MODIFIED TO ENSURE THAT INTESTINAL SPECIMENS ARE COLLECTED & FIXED w/in A FEW MINUTES AFTER EUTH, & APPROPRIATE FRESH & UNCONTAMINATED SAMPLES ARE COLLECTED FOR ETIOLOGICAL INVESTIGATION
74
Q

Who does Enterotoxigenic colibacillosis (ETEC) affect?

A
  • most commonly piglets & calves (& occasionally lambs) during the first weeks of life
  • may be fatal
75
Q

What is the pathogenesis of enterotoxigenic collibacillosis?

A
  • E. coli attach to surface enterocytes by a variety of fimbriae (ex: F4 in piglets & F5 in calves) & produce enterotoxins (Ex: ST, LT) that induce the secretion of Na & Cl into the intestinal lumen
  • water is drawn into the intestine by secreted ions
  • accordingly, this D+ is called secretory
  • absorptive function of the enterocytes persists
76
Q

What are the clinical signs of enterotoxigenic collibacillosis?

A
  • D+ is voluminous, yellow to white, & watery
  • neonates are severely dehydrated (sunken eyes)
  • diarrheic feces around perineum
77
Q

what would we see on necropsy w/ enterotoxigenic collibacillosis?

A
  • small intestines are dilated, flaccid, & filled w/ yellow fluid
  • chyle is present in the mesenteric lymphatic vessels similar to animals w/o enteric disease, indicating that absorption proceeds normally unlike the malabsorptive D+
  • subgrossly, intestinal villi are present & not affected
78
Q

How do we diagnose enterotoxigenic collibacillosis?

A
  • preliminary diagnosis may be based on evidence of severe dehydration, D+, & mortality together w/ the presence of chyle in the mesenteric lymphatics & intact villi (no atrophy) observed subgrossly during necropsy
  • histo on formalin fixed (not autolysed) small intestines: intestinal mucosa is normal; the only change is bacterial presence on the luminal surface of the enterocytes
  • bacterial culture of intestinal contents & PCR demonstration of genes for fimbria & toxins
79
Q

Who do rotaviruses cause malabsorptive D+ in?

A
  • calves, piglets, lambs, & foals during the first few weeks of life
  • each sp of animal has its specific rotavirus & they are not cross-infective
  • human rotavirus kills a million children each year in developing countries
80
Q

what are the clinical signs of rotavirus enteritis?

A
  • neonates are dehydrated, weak, have yellow watery D+
  • not fatal D. However, mortality occurs when there is a co-infection w/ other pathogens (ex: ETEC)
81
Q

what is the pathogenesis of rotavirus enteritis?

A
  • rotavirus targets the most mature villus enterocytes (distal ~1/2 of villus)
  • sloughing of injured enterocytes results in moderate villus atrophy
82
Q

How do we diagnose rotavirus enteritis?

A

histo (moderate villus atrophy) & IHC on formalin fixed (not autolysed) small intestines

83
Q

Who do coronaviruses affect?

A
  • cause malabsorptive D+ in calves & piglets during the 1st few wks of life
  • in pigs it is called transmissible gastroenteritis (TGE)
84
Q

What is the pathogenesis of coronavirus enteritis?

A
  • coronavirus targets all enterocytes on the entire villi, therefore villous atrophy is severe resulting in severe diarrhea that may be fatal in neonates
  • ‘naked adjacent villi’ w/ exposed basement mbs may adhere & fuse, resulting not only in villous atropy but also in villous fusion, preventing the reformation of normal villi if the animal survives
  • this may be the reason that affected surviving animals remain chronic “poor doers”
85
Q

What are the clinical signs of coronavirus enteritis?

A
  • neonates may be severely dehydrated & weak
  • yellow watery D+
  • Neonatal morbidity & mortality in susceptible herds approach 100%
86
Q

How do we diagnose coronavirus enteritis?

A
  • preliminary dx may be based on the presence of villous atrophy observed subgrossly during necropsy
  • histo (severe villous atrophy) & IHC on formalin fixed (not autolysed) small intestines
87
Q

How does coronavirus enteritis affect older pigs?

A
  • in naive pigs older than 3 wks, transmissible gastroenteritis virus (TGE) infection causes transient clinical signs w/ eventual recovery
  • sows are susceptible to the virus, and morbidity among the sows is 100%, but the clinical signs are mild & transient (fever, V+, inappetence, & agalactia), & none die
  • immunity is solid & transferable through colostrum
88
Q

What do feline & canine coronaviruses cause?

A
  • mild self-limiting transient D+ in young animals
89
Q

What is porcine epidemic D+?

A
  • caused by a coronavirus, which is distinguishable from transmissible gastroenteritis of swine (TGE) only by lab tests
  • based on clinical presentations, it is difficult to distinguish PED from TGE
  • 1st outbreaks in the USA (2013) & Canada (2014) were characterized by explosive epidemics of D+ & V+ in all ages, w/ 90-95% mortality in suckling pigs
  • histo revealed sever atrophy of villi in all segments of the small intestines, but testing for rotaviruses & TGE virus were negative
  • CONFIRMED + CASE: atrophic enteritis demonstrated by histo & + for PED virus by PCR or virus isolation
90
Q

What is cryptosporidiosis? who does it infect?

A
  • Cryptosporidium parvum is a cause of malabsorptive D+ in calves & occasionally in lambs & foals
  • ubiquitous protozoan pathogen of mammals
  • it is a significant cause of municipal water contamination - zoonosis
91
Q

What is the pathogenesis of cryptosporidiosis?

A
  • cryptosporidia attach to surface epithelial cells of the stomach, small intestine, or colon, & displace & damage the microvilli
  • ultimate damage to & loss of enterocytes results in villous atrophy
92
Q

What are the clinicals signs of cryptosporidiosis?

A
  • watery D+ & dehydration
  • usually self-limiting & non-fatal, unless accompanied w/ co-infections w/ other pathogens or immunodeficiency
93
Q

What would you see on necropsy w/ cryptosporidiosis?

A
  • affected portions of the GI tract contain watery fluid
  • cryptosporidia may be observed in intestinal scrapings stained w/ Giemsa or acid fast
94
Q

How do we diagnose cryptosporidiosis?

A
  • parasitology: demonstration of large numbers of oocytes in feces
  • histo: villous atrophy w/ large number of Cryptosporidia in formalin fixed (not autolysed) intestines
95
Q
A

Sys Path II (11 decks)

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